Dr. Kellman

Butyrate, oxalates and sleep are all closely tied to the health of the microbiome. Here are a few snippets from some of my favorite interviews on the Microbiome Medicine Summit 2:

Healthy Messages from Body to Brain: Dr. David Perlmutter

Butyrate is one of the 3 very important short chain fatty acids that are made in the gut: butyrate, propionate, and acetic acid are the products of the healthy bacteria.

And it turns out that butyrate has some far reaching effects in the body. It acts as a fuel for the cells that line the gut. It acts as a modulator of our gene expression, a fancy term called histone deacetylase inhibitor, but it changes the expression of our DNA.

It regulates the leakiness of the gut lining. It regulates the leakiness of the blood brain barrier, and it also simulates specific receptors on immune cells called G protein receptors that code for things like the formation of inflammatory chemicals, so it has wide-ranging effects.

We can increase our butyrate by having healthier gut bacteria. We can eat butyrate in certain foods. It comes from the word butter; butter is probably nature’s richest source of butyrate.

Special Diets & the Microbiome: Julie Matthews

What’s interesting about oxalates is they can affect and actually damage mitochondria. Mitochondria, those little powerhouses in the cell, there are millions and millions of those going on every second that supply our entire body, every cell, every organ of our body with energy at every second.

Issues with mitochondria are very common not only on autism but variety of conditions including fibromyalgia and all sorts of pain-related condition. And we often see when people have mitochondrial issues that they have issues with three or more systems. So if they’ve got issues with their gut and maybe something in their central nervous system or their immune system.

And interestingly, there is a microbiome connection with oxalates as well. And what that is, is that oxalates have to be broken down by good bacteria, particularly there is a bacteria called Oxalobacter formigenes and its job is to break down oxalates. There are other bacteria. There are Lactobacillus bacteria that can help break down oxalates, as well. Oxalobacter is particularly sensitive to antibiotics. Even a single round of antibiotics can really damage this population, sometimes not only for the short-term but sometimes for the longer term, particularly when someone has had multiple rounds.

Cleansing the Microbiome: Donna Gates

People probably don’t have this picture of the microbiome in their mind. But it’s very dynamic. It changes all the time. If you change your diet, your microbiome is going to change. If you travel, it’s going to change because you’re eating different foods and so on.

It’s also very cyclical. So, what happens at night when we go to sleep—the microbiome changes. There are certain microbes that become dormant—become quiet. And they don’t do anything much. And other ones become very active at night when we’re sleeping.

What happens if you have sleep disorders—like sleep apnea, for example, where you’re not breathing well at night—that’s going to change the diversity of the microbes in your gut. So, you want to correct sleep disorders.

You may not realize that when you don’t sleep, you’re harming the microbes in your gut. And you’re allowing the pathogenic crypts to have a heyday down in the gut. So, sleep is very important, very much connected to the microbiome.

Dr. Jill Carnahan’s interview on the Microbiome Medicine Summit 2 covers cutting edge new information about Alzheimer’s disease, based on the work and research of Dr. Dale Bredesen. They start with the gut-brain connection and Dr. Carnahan shares this:

we used to think of early-onset cognitive decline and dementias and mood disorders as being in their own bucket. And so, we saw psychiatrists or neurological doctors or neurologists to treat those diseases. And now we’re finding as we knew for several years with functional medicine that, obviously, it’s all connected.

And the gut is especially important because this reservoir holds so many of our microbes and possibly pathogens and that speaks to the brain through the vagus nerve and through cytokines and through inflammatory molecules of all types.

And so, this conversation between our gut and our brain is very profound and has a huge impact on things like multiple sclerosis or dementia, Alzheimer’s, or even things like bipolar disorder, schizophrenia, depression, anxiety, and sleep disorders.

So what we’re finding is by addressing the immune system and the gut which are intricately connected, we can often get profound effects on areas in the body that are far from that, like the brain.

Dr. Kellman asks Dr. Carnahan to share a study that will be the slam dunk for really believing in this connection and she mentions a paper titled Microbes and Alzheimer’s Disease. It cites pathogens like herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete which can affect the brain and play a role in Alzheimer’s disease.

Dr. Carnahan then covers Dr. Dale Bredesen’s subtypes of early-onset dementia which allows you to treat the root cause and actually reverse symptoms. She goes into it in great detail so I’m going to give you the summary version here:

Type #1 is inflammatory

This could be from inflammation or infections or other poor dietary habits. And that’s where the microbiome could play into that.

You might see elevated CRP, IL-6, TNF-alpha. You might see a low albumin to globulin ratio. You might see high homocysteine, hypothyroid, elevated cortisol

Type #2 is atrophic: So that’s someone who loses their trophic factor of support like estrogen, testosterone, insulin, and vitamin D3.

And often, these type 1s and type 2s actually have ApoE-4 double mutations which are higher risk for Alzheimer’s.

Type #3 is toxic:

Toxic mold exposure, biotoxins from Lyme disease, or heavy metals or other chemicals.

Often these chemicals will act on the tight junctions of the gut and increase permeability. And then that permeability leads to massive endotoxemia.

Younger onset of symptoms (like 40s and 50s) and reversible once you find and remove the root cause

Type #4 is vascular: inflammation of the blood vessels, high homocysteine

Type #5 is traumatic: wrestlers or boxers or football players that have had multiple head injuries or trauma.

By addressing the various root causes, Dr. Bredesen reports a reduction and in some instances reversal of dementia symptoms.

Of course, we know anxiety is common when it comes to Alzheimer’s and dementia. By addressing many of these above root causes we’re also able to reduce anxiety symptoms at the same time.

It was a fascinating interview and I hope you enjoy it as much as I did. I learned a great deal and find it very useful to group the symptoms into types.

There does seem to be one aspect that Dr. Carnahan didn’t address and I haven’t seen it covered in Dr. Bredesen’s papers: the impact of benzodiazepines on dementia and Alzheimer’s disease. There is conflicting research on this but I feel there is enough research that does show a correlation – enough for us to be concerned. Here is a recent paper looking at high-dose benzodiazepine use in Chinese patients, supporting an association.

Our results suggest that benzodiazepine use is significantly associated with dementia risk. However, observational studies cannot clarify whether the observed epidemiologic association is a causal effect or the result of some unmeasured confounding variable. Therefore, more research is needed.

This may likely fall under type #3 (toxic). I plan to reach out to them as a follow-up.

UPDATE: May 9, 2017. I did hear back from Dr. Carnahan and she shared that she always discusses history and physical and lab testing, and history of benzodiazepine use or other neuroactive substances.

Anxiety and depression are very common symptoms of SIBO or small intestinal bacterial overgrowth and Dr. Alison Siebecker, one of the speakers on the Microbiome Medicine Summit 2 shares this about anxiety and SIBO:

I see their anxiety resolving, going way down, once the SIBO is treated. I see a lot of very anxious SIBO patients. It’s caused by one of the mechanisms. It’s the cell wall of the bacteria. The LPS otherwise known as endotoxins, that can stimulate inflammatory cytokines and these affect mood.

She discusses some of the common causes of SIBO or small intestinal bacterial overgrowth:

So we’re talking about the deficiency of migrating motor complex. And this is a form of like peristalsis or motility that occurs in the small intestine itself. And its whole purpose is to clear the small intestine of bacteria, believe it or not, and cellular debris, any leftover food. Because it works in between meals, it works when we’re actually fasting, so in between meals and then overnight when we’re sleeping.

It’s kind of like—it’s called the housekeeper wave. It comes and sweeps and cleans up after we eat. So what can happen for really the predominant amount of people is that this motility becomes deficient. Or it doesn’t function very well. Now, there are a lot of things that could cause this motility to get deficient. There are many diseases, some of them quite common, like diabetes, hypothyroid.

We’ve got drugs that can slow it like opioid painkillers, opioid narcotics, very common for a lot of people. I do see a lot of people with SIBO after they take narcotic or painkillers, for instance for like a knee surgery or maybe they had gallstones or kidney stones. They had to take them for awhile—back pain, things like that. This can slow the migrating motor complex and allow SIBO to develop.

But probably the most common reason of all is from an acute disease, which is food poisoning or otherwise known as acute gastroenteritis, and here we’re talking about the bacterial type.

And this is what’s really revolutionary to me about SIBO and what we’ve learned. This is the work of Dr. Pimentel and associates many years figuring this out.

She shares how the toxin secreted by the bacteria (from the food poisoning) causes an autoimmune-type reaction

What happens is, in bacterial food poisoning, all the bacteria that cause this secrete—they are pathogenic bacteria. And they secrete a toxin. And it’s all the same toxin, CDT, which stands for cytolethal distending toxin.

Well, it turns out a portion of this toxin, the B portion—it’s just named B. It has an A, B, and C part. The B portion looks like a protein that’s on one of these very important nerve cells, as you just mentioned, that sort of generates this migrating motor complex.

So what happens is through a case of mistaken identity—or we could call it friendly fire. Or we could call it molecular mimicry. These are all words for the initiation of an autoimmune process through that because this protein on our nerve cell looks like the toxin. Our immune system gets triggered into damaging and fighting against our own nerve cells.

So it damages our nerve cells. And then the migrating motor complex can’t be produced properly. And what studies have shown is that the damage has to reach a certain threshold where these cells are diminishing. And then that will really, really slow down the migrating motor complex. And at a certain level there, the SIBO will develop.

The rates are pretty high – anywhere from 10% to 20% of people – who get food poisoning go on and get SIBO.

And she shares about the IBSchek test that

checks for the antibodies against that toxin, CDT-B, and the protein, which is actually called the vinculin, the protein that was on the nerve cells.

I always enjoy hearing Dr. Siebecker’s interviews and learn something new every time. This one was no exception!

We know that one of your greatest ally in health is your microbiome – the trillions of bacteria that are the control center of your health! But sometimes your microbiome can actually cause problems. One way to improve the microbiome is via microbiota transfer therapy (MTT), also called fecal microbiota transplant (FMT).

During the interview Dr. Kellman asked what bacterial changes were observed and I didn’t have the study on hand. I looked it up after the interview and this is what they report

Specifically, overall bacterial diversity and the abundance of Bifidobacterium, Prevotella, and Desulfovibrio among other taxa increased following MTT, and these changes persisted after treatment stopped (followed for 8 weeks).

Also

following MTT, the relative abundance of Bifidobacterium significantly increased fourfold and became comparable to its relative abundance in neurotypical children

They conclude that the MTT

shifted gut microbiota of children with ASD toward that of neurotypical children … consistent with the hypothesis that gut microbiota may be at least partially responsible for GI and ASD symptoms

Research just published last month reports similar results with digestive issues and anxiety. Germ-free mice were given the fecal microbiota from healthy control individuals or IBS patients with diarrhea, with or without anxiety. They found that the microbiota profiles in the mice matched the microbiota profiles of the human donors, affecting their digestive function and anxiety levels! I’ll share more on this study in a future blog post.